Homo sapiens
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PROVIDER: PRJNA243266 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression profile of PC-3-derived cell lines after transendothelial migration
| PRJNA111795 | ENA
Project description:Metastatic colonization involves cancer cell lodgment or adherence in the microvasculature and subsequent migration of those cells across the endothelium into a secondary organ site. To study this process further, we analyzed both in vitro and in vivo migration of human PC-3 prostate cancer cells . We isolated 6 subpopulation of cells: TEM4-18 were isolated from in vitro transendothelial migration of PC-3 cells; GS672.Ug, GS683.LALN and JD1203.Lu are single passaged in vivo cell lines from TEM4-18; GS689.Li and GS694.LAd are twice passaged in vivo cell lines from PC-3 cells. All the subpopulations crossed an endothelial barrier more efficiently and more aggressive in a murine metastatic colonization model than parental PC-3 cells. Microarray and FACS analysis of these cells showed that the expression of many genes previously associated with leukocyte trafficking and cancer cell extravasation were either unchanged or down-regulated. These cells exhibited characteristic molecular markers of an epithelial-to-mesenchymal transition, including frank loss of E-cadherin expression and upregulation of the E-cadherin repressor ZEB1. We used microarray to detail the global programme of gene expression underlying cancer metastasis. We wanted to compare the expression profiles of cells that had undergone transendothelial migration in vitro or metastasis in vivo. TEM4-18 was generated from the parental PC-3 that was plated onto a confluent human microvascular endothelial cell line from the lung and allowed to migrate across this monolayer. GS672.Ug were isolated from urogenital after intravenous injection of PC-3 cells. GS683.LALN and JD1203.Lu were isolated from lung after intravenous injection of TEM-418 cells. JD549.Ki were isolated from kidney after intravenous injection PC-3 cells. GS689.Li and GS694.LAd were isolated from liver and left adrenal after intravenous injection of JD549.Ki. All the cell lines are analyzed once except duplicate for TEM4-18 in this experiment for a total of 7 samples in this microarray. All other five sublines were then compared to TEM4-18 cells for changes in gene expression.
2014-04-10 | E-GEOD-56410 | biostudies-arrayexpress
Project description:Metastatic colonization involves cancer cell lodgment or adherence in the microvasculature and subsequent migration of those cells across the endothelium into a secondary organ site. To study this process further, we analyzed transendothelial migration of human PC-3 prostate cancer cells in vitro. We isolated a subpopulation of cells, TEM4-18, that crossed an endothelial barrier more efficiently, but surprisingly, were less invasive than parental PC-3 cells in other contexts in vitro. Importantly, TEM4-18 cells were more aggressive than PC-3 cells in a murine metastatic colonization model. Microarray and FACS analysis of these cells showed that the expression of many genes previously associated with leukocyte trafficking and cancer cell extravasation were either unchanged or down-regulated. TEM4-18 cells exhibited characteristic molecular markers of an epithelial-to-mesenchymal transition (EMT), including frank loss of E-cadherin expression and upregulation of the E-cadherin repressor ZEB1. Silencing ZEB1 in TEM4-18 cells resulted in increased E-cadherin and reduced transendothelial migration. TEM4-18 cells also express N-cadherin, which was found to be necessary, but not sufficient for increased transendothelial migration. Our results extend the role of EMT in metastasis to transendothelial migration and implicate ZEB1 and N-cadherin in this process in prostate cancer cells. Experiment Overall Design: We wanted to compare the expression profiles of cells that had undergone transendothelial migration. The parental, and reference cell line, PC-3 was plated onto a confluent human microvascular endothelial cell line from the lung and allowed to migrate across this monolayer. A new cell line, TEM4-18, was isolated from this experiment. We also performed this experiment a second time to isolate a biological replicate of the TEM4-18 cell line, termed TEM2-5. All 3 cell lines, PC-3, TEM4-18, and TEM2-5 are analyzed as replicates in this experiment for a total of 6 samples in this microarray. Both TEM4-18 and TEM2-5 were then compared to PC-3 cells for changes in gene expression.
2009-01-25 | E-GEOD-14405 | biostudies-arrayexpress
Project description:Metastatic colonization involves cancer cell lodgment or adherence in the microvasculature and subsequent migration of those cells across the endothelium into a secondary organ site. To study this process further, we analyzed both in vitro and in vivo migration of human PC-3 prostate cancer cells . We isolated 6 subpopulation of cells: TEM4-18 were isolated from in vitro transendothelial migration of PC-3 cells; GS672.Ug, GS683.LALN and JD1203.Lu are single passaged in vivo cell lines from TEM4-18; GS689.Li and GS694.LAd are twice passaged in vivo cell lines from PC-3 cells. All the subpopulations crossed an endothelial barrier more efficiently and more aggressive in a murine metastatic colonization model than parental PC-3 cells. Microarray and FACS analysis of these cells showed that the expression of many genes previously associated with leukocyte trafficking and cancer cell extravasation were either unchanged or down-regulated. These cells exhibited characteristic molecular markers of an epithelial-to-mesenchymal transition, including frank loss of E-cadherin expression and upregulation of the E-cadherin repressor ZEB1. We used microarray to detail the global programme of gene expression underlying cancer metastasis.
2014-04-10 | GSE56410 | GEO
Project description:S100P is a metastasis-associated gene that facilitates transendothelial migration of pancreatic cancer cells [HG-U133_Plus_2]
2025-01-24 | E-GEOD-19278 | ExpressionAtlas
Project description:Metastatic colonization involves cancer cell lodgment or adherence in the microvasculature and subsequent migration of those cells across the endothelium into a secondary organ site. To study this process further, we analyzed transendothelial migration of human PC-3 prostate cancer cells in vitro. We isolated a subpopulation of cells, TEM4-18, that crossed an endothelial barrier more efficiently, but surprisingly, were less invasive than parental PC-3 cells in other contexts in vitro. Importantly, TEM4-18 cells were more aggressive than PC-3 cells in a murine metastatic colonization model. Microarray and FACS analysis of these cells showed that the expression of many genes previously associated with leukocyte trafficking and cancer cell extravasation were either unchanged or down-regulated. TEM4-18 cells exhibited characteristic molecular markers of an epithelial-to-mesenchymal transition (EMT), including frank loss of E-cadherin expression and upregulation of the E-cadherin repressor ZEB1. Silencing ZEB1 in TEM4-18 cells resulted in increased E-cadherin and reduced transendothelial migration. TEM4-18 cells also express N-cadherin, which was found to be necessary, but not sufficient for increased transendothelial migration. Our results extend the role of EMT in metastasis to transendothelial migration and implicate ZEB1 and N-cadherin in this process in prostate cancer cells.
2009-01-15 | GSE14405 | GEO
Project description:Gene expression profile of two Ara-C-resistant cell lines
2015-09-07 | E-GEOD-18322 | ExpressionAtlas
Project description:Gene expression profile of acute lymphoblastic leukemia cell lines treated with panobinostat
2025-01-24 | E-GEOD-26790 | ExpressionAtlas
Project description:The aberrant activation of HER2 has a pivotal role in bone metastasis implantation and progression in several tumor types, in-cluding prostate cancer (PC). Trastuzumab and other anti-HER2 therapies, such as lapatinib, have been used in human breast cancer HER2 positive. Although HER2 overexpression has been reported in PC, anti-HER2 therapy response has revealed conflicting results. We investigated the potential of lapatinib in inhibiting cell migration and inducing apoptosis in two human (LNCaP and PC3) and two canine PC cell lines (PC1 and PC2). Cell migration and apoptosis were evaluated by Annexin V/PI analysis after lapatinib treatment. The transcriptome analysis of all cell lines before and after treatment with lapatinib was also performed. We found increased apoptosis and migration inhibition in LNCaP cells (androgen-sensitive cell line), while PC1, PC2, and PC3 cells showed no alterations after the treatment. The transcriptome analysis of LNCaP and PC3 cell lines showed 158 dysregulated transcripts in common, while PC1 and PC2 cell lines presented 82. At the doses of lapatinib used, we observed transcriptional modifications in all cell lines. PI3K/AKT/mTOR pathway were enriched in human PC cells, while canine PC cells showed en-richment of tyrosine kinase antitumor response and HER2-related pathways. In canine PC cells, the apoptosis failed after lapatinib treatment, possibly due to the downregulation of MAPK genes. Prostate cancer cells insensitive to androgens may be resistant to lapatinib through PI3K gene dysregulation. The association of lapatinib with PI3K inhibitors may provide a more effective anti-tumor response and clinical benefits to PC patients.
2023-11-30 | E-MTAB-13551 | biostudies-arrayexpress
Project description:The aberrant activation of HER2 has a pivotal role in bone metastasis implantation and progression in several tumor types, in-cluding prostate cancer (PC). Trastuzumab and other anti-HER2 therapies, such as lapatinib, have been used in human breast cancer HER2 positive. Although HER2 overexpression has been reported in PC, anti-HER2 therapy response has revealed conflicting results. We investigated the potential of lapatinib in inhibiting cell migration and inducing apoptosis in two human (LNCaP and PC3) and two canine PC cell lines (PC1 and PC2). Cell migration and apoptosis were evaluated by Annexin V/PI analysis after lapatinib treatment. The transcriptome analysis of all cell lines before and after treatment with lapatinib was also performed. We found increased apoptosis and migration inhibition in LNCaP cells (androgen-sensitive cell line), while PC1, PC2, and PC3 cells showed no alterations after the treatment. The transcriptome analysis of LNCaP and PC3 cell lines showed 158 dysregulated transcripts in common, while PC1 and PC2 cell lines presented 82. At the doses of lapatinib used, we observed transcriptional modifications in all cell lines. PI3K/AKT/mTOR pathway were enriched in human PC cells, while canine PC cells showed en-richment of tyrosine kinase antitumor response and HER2-related pathways. In canine PC cells, the apoptosis failed after lapatinib treatment, possibly due to the downregulation of MAPK genes. Prostate cancer cells insensitive to androgens may be resistant to lapatinib through PI3K gene dysregulation. The association of lapatinib with PI3K inhibitors may provide a more effective anti-tumor response and clinical benefits to PC patients.
2023-11-30 | E-MTAB-13552 | biostudies-arrayexpress